ArticlePNAS nexus2023
Maternal-derived galectin-1 shapes the placenta niche through Sda terminal glycosylation: Implication for preeclampsia.
Article in PNAS nexus, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Insights into Reproductive Immunology and Placental Pathology, 2nd Edition.International journal of molecular sciences · 2026Article
- Maternal Galectins and Glucose Regulation in Pregnancy: Chronic vs. Acute Metabolic Adaptations.Diabetes & metabolism journal · 2026Article
- Abnormal Galectin Signaling in the Pathomechanisms of Placental Dysfunction in Gestational Diabetes Mellitus.International journal of molecular sciences · 2026Review
- Maternal Serum Galectin-1 in the First Trimester as a Potential Biomarker for Early Prediction of Pre-Eclampsia: A Prospective Study.Medical science monitor : international medical journal of experimental and clinical research · 2025Article
- Multi-omic insights of preeclampsia and cardiovascular health outcomes.Communications medicine · 2025Review
- Maternal and placental galectins: key players in the feto-maternal symbiotic tango.Seminars in immunopathology · 2025Review
- Fetal growth restriction induced by maternal gal-3 deficiency is associated with altered gut-placenta axis.Cell death & disease · 2024Article
- A Narrative Review on the Pathophysiology of Preeclampsia.International journal of molecular sciences · 2024Review
- Article
- Impact of Gene Duplication of B4GALNT2 in Pigs for Xenotransplantation- Technical & Practical.XenotransplantationArticle
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 3 countries.
Funding
Abstract
Placental abnormalities cause impaired fetal growth and poor pregnancy outcome (e.g. preeclampsia [PE]) with long-lasting consequences for the mother and offspring. The molecular dialogue between the maternal niche and the developing placenta is critical for the function of this organ. Galectin-1 (gal-1), a highly expressed glycan-binding protein at the maternal-fetal interface, orchestrates the maternal adaptation to pregnancy and placenta development. Down-regulation or deficiency of gal-1 during pregnancy is associated with the development of PE; however, the maternal- and placental-derived gal-1 contributions to the disease onset are largely unknown. We demonstrate that lack of gal-1 imposes a risk for PE development in a niche-specific manner, and this is accompanied by a placental dysfunction highly influenced by the absence of maternal-derived gal-1. Notably, differential placental glycosylation through the Sda-capped N-glycans dominates the invasive trophoblast capacity triggered by maternal-derived gal-1. Our findings show that gal-1 derived from the maternal niche is essential for healthy placenta development and indicate that impairment of the gal-1 signaling pathway within the maternal niche could be a molecular cause for maternal cardiovascular maladaptation during pregnancy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.